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Title: | Epigallocatechin-3-gallate reduces the proliferation of benign prostatic hyperplasia cells via regulation of focal adhesions |
Authors: | Soya, Elif Korkmaz, Mehmet Uludağ Üniversitesi/Fen-Edebiyat Fakültesi/Moleküler Biyoloji ve Genetik Bölümü. Tepedelen, Burcu Erbaykent AAH-6436-2021 47860936500 |
Keywords: | Pharmacology & pharmacy Research & experimental medicine BPH Cytoskeleton EGCG F-Actin FAK Paxillin Green-tea Epithelial-cells Metabolic syndrome Growth-factor Cancer risk Expression Migration Kinase Inhibition Apoptosis |
Issue Date: | 11-Oct-2017 |
Publisher: | Elsevier |
Citation: | Tepedelen, B. E. vd. (2017). ''Epigallocatechin-3-gallate reduces the proliferation of benign prostatic hyperplasia cells via regulation of focal adhesions''. Life Sciences, 191, 74-81. |
Abstract: | Aims: Benign prostatic hyperplasia (BPH) is the most common urological disease that is characterized by the excessive growth of prostatic epithelial and stromal cells. Pharmacological therapy for BPH has limited use due to the many side effects so there is a need for new agents including natural compounds such as epigallocatechin-3-gallate (EGCG). This study was undertaken to assess the role of EGCG, suppressing the formation of BPH by reducing inflammation and oxidative stress, in cytoskeleton organization and ECM interactions via focal adhesions. Main methods: We performed MTT assay to investigate cell viability of BPH-1 cells, wound healing assay to examine cell migration, immunofluorescence assay for F-actin organization and paxillin distribution and finally immunoblotting to investigate focal adhesion protein levels in the presence and absence of EGCG. Key findings: We found that EGCG inhibits cell proliferation at the concentration of 89.12 mu M, 21.2 mu M and 2.39 mu M for 24, 48 and 72 h, respectively as well as inhibitory effects of EGCG on BPH-1 cell migration were observed in a wound healing assay. Furthermore, it was determined by immunofluorescence labeling that EGCG disrupts F-actin organization and reduces paxillin distribution. Additionally, EGCG decreases the activation of FAK (Focal Adhesion Kinase) and the levels of paxillin, RhoA (Ras homolog gene family, member A), Cdc42 (cell division cycle 42) and PAK1 (p21 protein-activated kinase 1) in a dose-dependent manner. Significance: For the first time, by this study, we found evidence that BPH-1 cell proliferation could be inhibited with EGCG through the disruption of cytoskeleton organization and ECM interactions. Consequently, EGCG might be useful in the prevention and treatment of diseases characterized by excessive cell proliferation such as BPH. |
URI: | https://doi.org/10.1016/j.lfs.2017.10.016 https://www.sciencedirect.com/science/article/pii/S0024320517305301 1879-0631 http://hdl.handle.net/11452/30518 |
ISSN: | 0024-3205 |
Appears in Collections: | Scopus Web of Science |
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